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goat anti rat vegf  (R&D Systems)


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    R&D Systems goat anti rat vegf
    Figure 3. Finerenone reduced <t>VEGF</t> and vascular leakage in (mRen-2)27 after 12 weeks of diabetes. D, diabetic. Veh, vehicle. Per, perindopril. Fin, finerenone. (A) Three-micrometer paraffin sections of retina immunolabeled with VEGF and counterstained with hematoxylin. GCL, ganglion cell layer. IPL, inner plexiform layer. INL, inner nuclear layer. Scale bar = 40 µm. Ganglion cells denoted by single asterisk (*). Glial cells denoted by double asterisks (**). (B) Quantitation of VEGF immunolabeling in the retina. * p < 0.05 to diabetic+vehicle. n = 4 to 5 rats per group. (C) Vitreal levels of albumin (ELISA). * p < 0.05 to non-diabetic and diabetic+vehicle. # p < 0.05 to non-diabetic. n = 7 to 8 rats per group. Values are mean ± SEM.
    Goat Anti Rat Vegf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 43 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/564-RV/pm36768656-149-21-26?v=R%26D+Systems
    Average 94 stars, based on 43 article reviews
    goat anti rat vegf - by Bioz Stars, 2026-08
    94/100 stars

    Images

    1) Product Images from "Finerenone, a Non-Steroidal Mineralocorticoid Receptor Antagonist, Reduces Vascular Injury and Increases Regulatory T-Cells: Studies in Rodents with Diabetic and Neovascular Retinopathy."

    Article Title: Finerenone, a Non-Steroidal Mineralocorticoid Receptor Antagonist, Reduces Vascular Injury and Increases Regulatory T-Cells: Studies in Rodents with Diabetic and Neovascular Retinopathy.

    Journal: International journal of molecular sciences

    doi: 10.3390/ijms24032334

    Figure 3. Finerenone reduced VEGF and vascular leakage in (mRen-2)27 after 12 weeks of diabetes. D, diabetic. Veh, vehicle. Per, perindopril. Fin, finerenone. (A) Three-micrometer paraffin sections of retina immunolabeled with VEGF and counterstained with hematoxylin. GCL, ganglion cell layer. IPL, inner plexiform layer. INL, inner nuclear layer. Scale bar = 40 µm. Ganglion cells denoted by single asterisk (*). Glial cells denoted by double asterisks (**). (B) Quantitation of VEGF immunolabeling in the retina. * p < 0.05 to diabetic+vehicle. n = 4 to 5 rats per group. (C) Vitreal levels of albumin (ELISA). * p < 0.05 to non-diabetic and diabetic+vehicle. # p < 0.05 to non-diabetic. n = 7 to 8 rats per group. Values are mean ± SEM.
    Figure Legend Snippet: Figure 3. Finerenone reduced VEGF and vascular leakage in (mRen-2)27 after 12 weeks of diabetes. D, diabetic. Veh, vehicle. Per, perindopril. Fin, finerenone. (A) Three-micrometer paraffin sections of retina immunolabeled with VEGF and counterstained with hematoxylin. GCL, ganglion cell layer. IPL, inner plexiform layer. INL, inner nuclear layer. Scale bar = 40 µm. Ganglion cells denoted by single asterisk (*). Glial cells denoted by double asterisks (**). (B) Quantitation of VEGF immunolabeling in the retina. * p < 0.05 to diabetic+vehicle. n = 4 to 5 rats per group. (C) Vitreal levels of albumin (ELISA). * p < 0.05 to non-diabetic and diabetic+vehicle. # p < 0.05 to non-diabetic. n = 7 to 8 rats per group. Values are mean ± SEM.

    Techniques Used: Immunolabeling, Quantitation Assay, Enzyme-linked Immunosorbent Assay

    Figure 5. Finerenone reduced retinal neovascularization, VEGF, and vascular leakage in mice with OIR at postnatal day 18. RA, room air control. Veh, vehicle. Fin, finerenone. (A) Retinal wholemounts labeled with FITC-isolectin to delineate retinal blood vessels in green. Top panels show whole retina. A quadrant of retina (yellow box) is magnified in the lower panel. Scale bar = 500 µm. Asterisks denote vaso-obliteration. Arrows denote neovascularization. (B) Quantitation of retinal neovascularization. * p < 0.05 to OIR+vehicle. n = 5 to 7 mice per group from 2 to 3 liters per group. (C) Retinal VEGF protein levels (ELISA). (D) Retinal VEGF mRNA levels. (E) Retinal vascular leakage (albumin ELISA). ** p < 0.01, **** p < 0.0001 to RA. # p < 0.05, ### p < 0.001 to OIR + vehicle (Kruskal–Wallis test). n = 5 to 8 mice per group from 2 to 3 litters of mice per group. Values are mean ± SEM.
    Figure Legend Snippet: Figure 5. Finerenone reduced retinal neovascularization, VEGF, and vascular leakage in mice with OIR at postnatal day 18. RA, room air control. Veh, vehicle. Fin, finerenone. (A) Retinal wholemounts labeled with FITC-isolectin to delineate retinal blood vessels in green. Top panels show whole retina. A quadrant of retina (yellow box) is magnified in the lower panel. Scale bar = 500 µm. Asterisks denote vaso-obliteration. Arrows denote neovascularization. (B) Quantitation of retinal neovascularization. * p < 0.05 to OIR+vehicle. n = 5 to 7 mice per group from 2 to 3 liters per group. (C) Retinal VEGF protein levels (ELISA). (D) Retinal VEGF mRNA levels. (E) Retinal vascular leakage (albumin ELISA). ** p < 0.01, **** p < 0.0001 to RA. # p < 0.05, ### p < 0.001 to OIR + vehicle (Kruskal–Wallis test). n = 5 to 8 mice per group from 2 to 3 litters of mice per group. Values are mean ± SEM.

    Techniques Used: Control, Labeling, Quantitation Assay, Enzyme-linked Immunosorbent Assay



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    Image Search Results


    Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

    Journal: Exploration of BioMat-X

    Article Title: Top2b regulates morphological and migratory properties of retinal progenitor cells in vivo and upon transplantable matrix substrates

    doi: 10.37349/ebmx.2025.101335

    Figure Lengend Snippet: Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

    Article Snippet: Approximately 600 μL of each growth factor vascular endothelial growth factor (VEGF; R&D Systems, Minneapolis, MN, USA, 564-RV), fibroblast growth factor-8 (FGF-8; Invitrogen, Carlsbad, CA, USA, PHG0184), and stromal derived factor 1-a (SDF-1a; Sigma Aldrich, St. Louis, MO, USA, SRP3276) was added to the bottom of separate transwell assays.

    Techniques: Cell Culture, Over Expression, Knockdown, Expressing, Derivative Assay

    Figure 4. Induction of VEGF (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 4. Induction of VEGF (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Cell Culture, In Vitro, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    Figure 5. Expression of VEGF in rupture-prone intracranial aneurysm (IA) lesions induced in rats. The images of immunofluorescent staining of IA lesions for VEGF (green), the marker for macrophages, CD68 (red), the marker for smooth muscle cell, α-smooth muscle actin (SMA, gray), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Magnified images corresponding to the square in the upper panels are shown in the lower panels. Scale bar: 50 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 5. Expression of VEGF in rupture-prone intracranial aneurysm (IA) lesions induced in rats. The images of immunofluorescent staining of IA lesions for VEGF (green), the marker for macrophages, CD68 (red), the marker for smooth muscle cell, α-smooth muscle actin (SMA, gray), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Magnified images corresponding to the square in the upper panels are shown in the lower panels. Scale bar: 50 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Expressing, Staining, Marker, Immunohistochemistry, Negative Control

    Figure 6. Expression of VEGF in human unruptured intracranial aneurysm (IA) lesions. The images of immunofluorescent staining of IA lesions for VEGF (green), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Scale bar: 50 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 6. Expression of VEGF in human unruptured intracranial aneurysm (IA) lesions. The images of immunofluorescent staining of IA lesions for VEGF (green), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Scale bar: 50 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Expressing, Staining, Immunohistochemistry, Negative Control

    Figure 7. VEGF-mediated induction of neovessels in subarachnoid space. The sheet for slow-release of VEGF or vehicle was placed on the right or the left of brain surface in the same rat (A) and the induction of vasa vasorum in subarachnoid space was examined. Asterisks indicate the sheets placed on brain surface. Scale bar: 1 mm. The macroscopic image of the brain surface (B) and the histopathological images from hematoxylin– eosin staining from specimen of vehicle- or VEGF-treated side (C) are shown. Dotted circles in (B) indicate the region where the sheet was placed. Noted the reddish appearance only in the VEGF-treated side indicating the induction of neovessels. Magnified images corresponding to the square in the left panels in (C) are shown on the right. Arrows indicate the neovessels induced in subarachnoid space. Scale bar: 50 μm. The images of immunofluorescent staining for the marker for smooth muscle cell, α-smooth muscle actin (SMA, red), nuclear staining by DAPI (blue), and merged images are shown in (D). Magnified images corresponding to the squares in the left panels are shown on the right. Scale bar: 100 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 7. VEGF-mediated induction of neovessels in subarachnoid space. The sheet for slow-release of VEGF or vehicle was placed on the right or the left of brain surface in the same rat (A) and the induction of vasa vasorum in subarachnoid space was examined. Asterisks indicate the sheets placed on brain surface. Scale bar: 1 mm. The macroscopic image of the brain surface (B) and the histopathological images from hematoxylin– eosin staining from specimen of vehicle- or VEGF-treated side (C) are shown. Dotted circles in (B) indicate the region where the sheet was placed. Noted the reddish appearance only in the VEGF-treated side indicating the induction of neovessels. Magnified images corresponding to the square in the left panels in (C) are shown on the right. Arrows indicate the neovessels induced in subarachnoid space. Scale bar: 50 μm. The images of immunofluorescent staining for the marker for smooth muscle cell, α-smooth muscle actin (SMA, red), nuclear staining by DAPI (blue), and merged images are shown in (D). Magnified images corresponding to the squares in the left panels are shown on the right. Scale bar: 100 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Staining, Marker